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探讨Src酪氨酸激酶抑制剂Ⅱ对Src蛋白及其下游信号的作用。半定量RT-PCR法检测Src酪氨酸激酶抑制剂Ⅱ处理后的人膀胱癌细胞T24各浓度组的c-Src、MMP9基因表达的变化情况,使用Western blot检测Src酪氨酸激酶抑制剂Ⅱ处理后T24细胞内的c-Src蛋白(包括其磷酸化与非磷酸化两种类型)表达情况。Src酪氨酸激酶抑制剂Ⅱ处理有下调后的人膀胱癌细胞T24各浓度组的c-Src mRNA的表达有下调;MMP9基因的表达有下调。处理后T24细胞内c-Src基因在蛋白表达水平上其磷酸化类型随Src酪氨酸激酶抑制剂Ⅱ浓度的增高表达逐渐下降,并且呈剂量效应关系。Src酪氨酸激酶抑制剂Ⅱ可能通过竞争Src蛋白磷酸化位点,使其不能激活,从而使得T24细胞增殖得到抑制,同时可能通过在转录水平上对MMP9的表达调节,使得MMP9基因在mRNA表达水平上下调,从而抑制T24细胞的增殖,诱导T24细胞凋亡,抑制或减弱人膀胱癌T24细胞的迁移/侵袭/转移的能力。
To investigate the effect of Src tyrosine kinase inhibitor II on Src protein and its downstream signal. Semi-quantitative RT-PCR method was used to detect the changes of c-Src and MMP9 gene expression in Src tyrosine kinase inhibitor II treated human bladder cancer cell line T24. The levels of Src tyrosine kinase inhibitor II The expression of c-Src protein (including both phosphorylation and non-phosphorylation) in T24 cells after treatment. Src tyrosine kinase inhibitor II treatment down-regulated the concentration of human bladder cancer T24 c-Src mRNA expression decreased; MMP9 gene expression down. The phosphorylation level of c-Src gene in T24 cells decreased gradually with the increase of Src tyrosine kinase inhibitor Ⅱ concentration and the dose-dependent manner. Src tyrosine kinase inhibitor Ⅱ may inhibit the proliferation of T24 cells by competing with the phosphorylation site of Src protein and inhibit the proliferation of T24 cells at the same time by regulating the expression of MMP9 at the transcriptional level, Down-regulated, thereby inhibiting the proliferation of T24 cells, inducing apoptosis of T24 cells and inhibiting or reducing the ability of human bladder cancer T24 cells to migrate / invade / metastasize.